DAPK2 Antibody (N_term) Blocking Peptide
- Known as:
- DAPK2 Antibody (N_term) Blocking Peptide
- Catalog number:
- BP7033a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- DAPK2 Antibody (N_term) Blocking Peptide
Related genes to: DAPK2 Antibody (N_term) Blocking Peptide
- Gene:
- DAPK2 NIH gene
- Name:
- death associated protein kinase 2
- Previous symbol:
- -
- Synonyms:
- DRP-1, MGC119312
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2016-10-05
Related products to: DAPK2 Antibody (N_term) Blocking Peptide
Related articles to: DAPK2 Antibody (N_term) Blocking Peptide
- Excess neutrophil apoptosis and the release of neutrophil extracellular traps (NETs) in systemic lupus erythematosus (SLE) lead to the accumulation of cell debris and the production of auto-antibodies targeting nuclear proteins and DNA. SLE neutrophil activation is regulated by changes in gene expression, notably expression of type I interferon-response genes and genes coding for granule proteins. This observational study measured both mRNA and small noncoding RNAs in SLE (n = 11) and healthy control (HC, n = 10) ultra-pure blood neutrophils to identify changes in expression that are involved in regulating neutrophil phenotype. Using RNAseq, we identified significant differential expression (DE) of 69 microRNAs, 63 other small noncoding RNAs, 236 piwiRNAs, and 83 tRNA fragments in SLE neutrophils compared to HC (false discovery rate [FDR] adj. P < 0.05). We also identified 78 significant alternative splicing events across 64 genes (FDR adj. P < 0.05, Δpercent spliced in (PSI) > 0.1 or < -0.1). Bioinformatic analysis of miRNA:mRNA DE genes predicted significant activation of autophagy, neutrophil degranulation, interferon alpha/beta signaling, and apoptosis pathways in SLE neutrophils. Translation and mRNA processing were predicted to be downregulated. microRNAs implicated in NETs production were miR-155-5p, miR-146a-5p, and miR-let-7b-5p (FDR adj. P < 0.05). SNORD89 was identified as a potential promoter of apoptosis in SLE neutrophils, along with alternative splicing of apoptosis genes myeloid cell leukemia-1 (MCL1), caspase-8 (CASP8), and death-associated protein kinase-2 (DAPK2) (FDR adj. P < 0.05). Our study, for the first time, describes dysregulated expression of small noncoding RNAs in SLE neutrophils and proposes noncoding RNA and alternative gene splicing as regulators of neutrophil-driven disease pathology in SLE. - Source: PubMed
Filbertine GraceChabronova AlzbetaLiu XuanHaldenby SamThomas Huw BattenMcLaren ZoePeffers Mandy JayneWright Helen Louise - Sepsis is associated with a pronounced but poorly understood endoplasmic reticulum stress (ERS) response. In this study, we found that death-associated protein kinase 2 (DAPK2), a calcium/calmodulin-regulated serine/threonine kinase, exhibits elevated expression in macrophages from patients with sepsis and from septic mice. Macrophage DAPK2 expression is transcriptionally upregulated through the activation of the Toll-like receptor 4 (TLR4)-myeloid differentiation primary response 88 (MyD88)-nuclear factor-κB (NF-κB) pathway. Macrophage-specific deletion of DAPK2 attenuated sepsis severity and mitigated the ERS response. Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), we identified heat shock protein family A member 5 (HSPA5) as a binding partner for DAPK2. Because DAPK2 function had been previously associated with the kinase activity, we speculated that it might control ERS of macrophages through HSPA5 phosphorylation. Further investigation indeed revealed that DAPK2 phosphorylates HSPA5 at serine-588, which promotes the proteasomal degradation of HSPA5 and subsequently leads to the activation of inositol-requiring enzyme 1α (IRE1α). Inhibition of HSPA5 exacerbated sepsis in mice with macrophage-specific DAPK2 deficiency; however, this effect was abrogated by the deactivation of IRE1α. In conclusion, our findings demonstrate that DAPK2 propagates macrophage ERS through the HSPA5-IRE1α axis during systemic infection, suggesting this pathway as a potential therapeutic target in sepsis. - Source: PubMed
Publication date: 2026/06/23
Ni YinTang Guo-ZhenQiu ChenZhu GeJin Shu-WenZhu Hai-PingMo Shi-JingFang Xiang-Ming - BackgroundmiRNAs are of interest due to have been involved in cancers such as colorectal cancer (CRC).ObjectiveTo explore the expression levels of miRNA-34a and miRNA-135b and whether they can be potential biomarker for early diagnosis of CRC.MethodsFifteen pairs newly diagnosed colorectal cancer and normal involved in the measurement of tissue and serum levels of miRNAs 34a and 135b and their target genes of SIRT1 and DAPK-1. We assessed the predictive value of these miRNAs utilizing the receiver operating characteristic curve.ResultsThe findings have shown that the miRNA-34a expression was significantly downregulated and miRNA-135b was upregulated in CRC tissues in comparison to their expression in adjacent normal tissue. This was additionally observed in the serum of the same CRC cases when compared to individuals without CRC. Furthermore, we found a significant increase in the level of SIRT-1 and a significant reduction in the expression level of DAPK-1 in CRC tissues compared to the adjacent normal tissue. The value of AUC was considerably high for the timely detection of CRC.ConclusionsWe found these miRNAs acting as potential non-invasive biomarkers for the early detection of CRC and in assessing the CRC risk within the general population. - Source: PubMed
Publication date: 2026/06/10
Karami RoyaNajafi ElahehBabaei AnahitaShahdoust ErfanShaghaghi AliAmiri-Dashatan NasrinMotlagh BehroozKoushki MehdiKhodabandehloo Hadi - Psoriasis is a chronic, immune-mediated disorder with an unmet need for effective treatments. To systematically prioritize therapeutic targets, we integrated proteome-wide Mendelian randomization (MR) with expression validation in blood/skin, genetic susceptibility analysis, differential gene expression (DGE) from bulk and single-cell RNA sequencing (scRNA-seq), colocalization, pathway enrichment, and protein-protein interaction analyses. - Source: PubMed
Si ShuchengWang XiaoxiaoZhan Siyan - Alzheimer's disease (AD) is a chronic progressive neurocognitive disorder manifested by increased production and deposition of amyloid beta (Aβ), abnormal tau phosphorylation, and formation of neurofibrillary tangles (NFTs). In addition, the disease progression is found to be associated with neuronal cell death, elevated levels of reactive oxygen species, mitochondrial dysfunction, and loss of synaptic plasticity in specific regions of the brain. AD is seventh leading cause of death and over more than 70%-80% of 57 million people having dementia develop AD worldwide. The disease population is also severely increasing at an alarming rate globally. The currently available treatment strategies remain insufficient to cure the disease because AD involves very complex pathways during its progression. Death-associated protein kinase 1 (DAPK1) is identified as a promising next-generation therapeutic drug target for the management of AD. It belongs to a family of serine/threonine kinases that influences different hypotheses involved in AD pathogenesis, such as tauopathies, Aβ hypothesis, redox, and autophagy pathways. In this review, we highlight the involvement of DAPK1 in various molecular pathways associated with AD pathogenesis and the crosstalk between DAPK1 and synaptic dysfunction and neuronal cell death implicated in AD. Moreover, the various small molecules, microRNAs, and phytoconstituents have been discussed, which have the potential to be developed as a treatment strategy targeting DAPK1-related pathological pathways in AD. - Source: PubMed
Publication date: 2026/05/22
Shukla ShashikeshSingh Rakesh Kumar